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CGA通过NF-κB信号通路减轻LPS诱导的BMECs炎症和乳脂肪减少。

CGA alleviates LPS-induced inflammation and milk fat reduction in BMECs through the NF-κB signaling pathway.

作者信息

Lyu Chen-Chen, Ji Xing-Yu, Che Hao-Yu, Meng Yu, Wu Hong-Yu, Zhang Jia-Bao, Zhang Yong-Hong, Yuan Bao

机构信息

College of Animal Science, College of Animal Sciences, Jilin Provincial Key Laboratory of Animal Model, Jilin University, Changchun, Jilin, PR China.

出版信息

Heliyon. 2024 Jan 21;10(3):e25004. doi: 10.1016/j.heliyon.2024.e25004. eCollection 2024 Feb 15.

Abstract

Mastitis is an easy clinical disease in dairy cows, which seriously affects the milk yield and quality of dairy cows. Chlorogenic acid (CGA), a polyphenolic substance, is abundant in Eucommia ulmoides leaves and has anti-inflammatory and anti-oxidative stress effects. Here, we explore whether CGA attenuated lipopolysaccharide (LPS)-induced inflammation and decreased milk fat in bovine mammary epithelial cells (BMECs). 10 μg/mL LPS was used to induce mastitis in BMECs. QRT-PCR, Western blotting, oil red O staining, and triglyceride (TG) assay were used to examine the effects of CGA on BMECs, including inflammatory response, oxidative stress response, and milk fat synthesis. The results showed that CGA repaired LPS-induced inflammation in BMECs. The expression of IL-6, IL-8, TNF-α, IL-1β, and iNOS was decreased, and the expression levels of CHOP, XCT, NRF2, and HO-1 were increased, which reduced the oxidative stress level of cells and alleviated the reduction of milk fat synthesis. In addition, the regulation of P65 phosphorylation by CGA suggests that CGA may exert its anti-inflammatory and anti-oxidative effects through the NF-κB signaling pathway. Our study showed that CGA attenuated LPS-induced inflammation and oxidative stress, and restored the decrease in milk fat content in BMECs by regulating the NF-κB signaling pathway.

摘要

乳腺炎是奶牛常见的临床疾病,严重影响奶牛的产奶量和牛奶品质。绿原酸(CGA)是一种多酚类物质,在杜仲叶中含量丰富,具有抗炎和抗氧化应激作用。在此,我们探究CGA是否能减轻脂多糖(LPS)诱导的炎症反应并减少牛乳腺上皮细胞(BMECs)中的乳脂肪含量。用10μg/mL LPS诱导BMECs发生乳腺炎。采用实时定量聚合酶链反应(QRT-PCR)、蛋白质免疫印迹法、油红O染色和甘油三酯(TG)测定法来检测CGA对BMECs的影响,包括炎症反应、氧化应激反应和乳脂肪合成。结果表明,CGA修复了LPS诱导的BMECs炎症反应。白细胞介素-6(IL-6)、白细胞介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和诱导型一氧化氮合酶(iNOS)的表达降低,而 Chop 同源蛋白(CHOP)、溶质载体家族7成员11(XCT)、核因子E2相关因子2(NRF2)和血红素加氧酶-1(HO-1)的表达水平升高,这降低了细胞的氧化应激水平并缓解了乳脂肪合成的减少。此外,CGA对P65磷酸化的调节表明,CGA可能通过核因子κB(NF-κB)信号通路发挥其抗炎和抗氧化作用。我们的研究表明,CGA通过调节NF-κB信号通路减轻了LPS诱导的炎症和氧化应激,并恢复了BMECs中乳脂肪含量的降低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b84/10838784/bfda4266fcf9/gr1.jpg

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